■    Compartment  syndrome remains one of the most devastating orthopedic conditions. The potential clinical sequelae and medicolegal implications  of  a  possible missed compartment syndrome make it one of the most important entities in all of orthopedic surgery.2

■  Compartment syndrome is a condition, with numerous causes, in which the pressure within the osteofascial compartment  rises to  a  level that  exceeds intramuscular  arteriolar pressure, resulting in decreased blood flow to the capillaries, decreased oxygen diffusion to the tissue, and ultimately cell death. This is a true orthopaedic emergency.

■    The  clinical  sequelae of  a  missed compartment syndrome can  be  life and  limb-threatening. Myonecrosis  can  lead  to acute renal failure and multiorgan failure if not appropriately managed.20

■    Richard  von Volkmann  first documented nerve injury and subsequent contracture from compartment syndrome in 1872 following a supracondylar fracture.

■    In 1906,  Dr.  Hildebrand  was the first to apply the term “Volkmann ischemic contracture” to define the end result of any untreated compartment syndrome.

■    In 1909, Dr. Thomas described the major causes of compartment syndrome (fractures being the predominant cause) after reviewing the 112 cases published up to that date.

■    The first to suggest that fasciotomy may help prevent contracture was Dr.  Murphy in 1914.

■    It was not until 1967 that Seddon, Kelly, and Whitesides described the existence of four compartments in the lower leg and the need to decompress more than just the anterior compartment.

■    Any situation that leads to an increased pressure within the compartment may result in a compartment syndrome.

■    The impermeable fascia prevents fluid from leaking out of the compartment and also prevents an increase in volume that could reduce pressure within the compartment.

■    The incidence of compartment syndrome is 7.3 per 100,000 males and 0.7 per 100,000 females.

■    In those cases, the most common cause was fracture followed by soft tissue injury.

■    McQueen et al found that the incidence of compartment syndrome was nearly equal for both highand low-energy injuries and that open wounds did not decompress the compartments and were not protective.13,14

■    This  chapter  describes acute  compartment  syndrome,  in contrast to exertional compartment syndrome.

■    Exertional compartment syndrome is a transient chronic condition  brought  on  by  exercise. Unlike  acute compartment syndrome, exertional compartment syndrome is not an emergency and  its  treatment is  beyond  the  scope of  this chapter.

■    The lower leg has four compartments: the anterior, lateral, superficial posterior, and deep posterior (FIG  1, Table 1).

■    The anterior compartment is bound anteriorly by fascia, lat-

erally by the anterior intermuscular septum, and posteriorly by the interosseous membrane between the fibula and tibia.

■    The four muscles in this compartment are the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius.

■    The  neurovascular  bundle  includes  the  deep  peroneal nerve and the anterior tibial artery.

■    The  deep peroneal nerve provides sensation to  the first dorsal web space of the foot and motor function to all the muscles in the anterior compartment.

■    The anterior tibial artery travels in this compartment just anterior to the tibiofibular interosseous membrane and continues in the foot as the dorsalis pedis artery.

■    The lateral compartment is bordered anteriorly by the fascia,  posteriorly by  the posterior intermuscular septum,  and medially by the fibula.

■    There are only two muscles of  the lateral compartment:

the peroneus longus and the peroneus brevis.

■    The major nerve supply to the lateral compartment is the superficial peroneal nerve, which supplies the two muscles of  the compartment.  The  nerve supplies sensation to  the dorsum of the foot, except the first dorsal web space.

■    Since the deep peroneal nerve courses proximally around the  fibular  head,  both  the  deep and  superficial peroneal nerves travel within this compartment.

■    There are no main vessels in this compartment, and the muscles receive their blood  supply from  the peroneal and anterior tibial arteries.

■    The deep posterior compartment contains the flexor digitorum  longus,  tibialis posterior, and  flexor  hallucis  longus muscles.

■    Although it is not considered a separate compartment, the tibialis posterior muscle can have its own fascial covering.

■    The deep posterior compartment contains the main neurovascular bundle of the posterior compartment, which consists of the tibial nerve, posterior tibial artery and vein, and peroneal artery and vein.

■    The superficial posterior compartment contains the gastrocnemius, soleus, and plantaris muscles, which are supplied by branches of  the tibial nerve, posterior tibial artery, and peroneal arteries.

■    There is no major artery that travels in this compartment.

■    Although the exact pathophysiology is not completely understood,  the premise of the syndrome is either a decrease in the space available for the tissues within the fixed compartment or an increase in the size of the tissues within the compartment.

FIG 1 • Cross-section of the lower leg  at mid-tibial level.

Table 1        Compartments of the Lower Leg

■    Either case can result in an increase in pressure above a critical value.

■    Increased fluid  content  and  swelling of  damaged muscles can be caused by the following:

■    Bleeding into the compartment (from fractures, large vessel injury, or bleeding disorders)

■    Fractures are the most common cause of compartment syndrome. It is estimated that 9.1%  of tibial plateau fractures develop compartment syndrome.3

■    Blunt  trauma is the second most common  cause,  accounting for 23% of cases.14

■  Increased capillary permeability (eg, burns, ischemia, exercise, snake bite, drug injection, intravenous fluids)

■    Decreased compartment size can be caused by the following:

■    Burns

■    Tight circumferential wrapping, dressings, casts

■    Localized external pressure, such as lying on the limb for an extended period of  time or from pressure on the “well leg”  in the lithotomy position on the fracture table

■    Elevated pressure prevents perfusion of the tissue from the capillaries and results in anoxia and necrosis.

■    The  impermeable fascia  prevents fluid  from  escaping, causing a rise in compartment pressure such that it exceeds

the pressure within the veins, resulting in their collapse or an increase in the venous pressure.17

■    The final event is cellular anoxia and necrosis.20

■    During necrosis there is an increase in the intracellular calcium concentration coupled with a subsequent shift of water into the tissue, causing the tissue to swell further, adding to the pressure.4 This “capillary  leakage”  adds to the increased pressure in the compartment, thus creating a vicious cycle.

■    The effects on muscle and nerve function are time-dependent.

■    Prolonged delay results in greater loss of function.

■    After sustained elevation of compartment pressures greater than 6 to 8 hours, nerve conduction is blocked.10 In an animal study, irreversible muscle damage occurred after 8 hours.22

■    The exact pressure at which change within the compartment occurs has been subject to debate and has evolved over time.

■    Initially, the pressure of 30 mm Hg was reported to be the maximum pressure above which irreversible muscle damage occurred.27

■    Currently,  clinicians have recognized the importance of the patient’s blood pressure when considering the compartment pressure and use an absolute difference between diastolic    blood    pressure   and    compartment   pressure   of

30 mm Hg  as a gauge.

■    Animal  studies have highlighted the importance of the systemic pressures relative to the compartment pressure.

■    Heckman  et al  found  that irreversible ischemic changes occurred  when  the  compartment  pressure was  elevated within 30 mm Hg  of the mean arterial pressure and within

20 mm Hg  of the diastolic pressure.27

■    Studies on limb ischemia at the University of Pennsylvania had similar conclusions.

■    They coined the term “delta P” referring to the difference between the mean arterial pressure minus the compartment pressure, with a lower number reflecting less blood flow.1

■    They found that cellular anoxia  and death occur with pressure within 20 mm Hg  of the mean arterial pressure; however, at  pressures within  40  mm  Hg  there was reduced oxygen tension but no evidence of anoxia,  and aerobic metabolism persisted.

■    McQueen and Court-Brown  used the cutoff of compartment pressure within 30 mm Hg of the diastolic blood pressure as a fasciotomy threshold.13

■    There were no adverse clinical  outcomes from not releasing compartments with pressures more than 30 mm Hg from the diastolic blood pressure, and this has come to be the value currently used most often as a threshold for compartment syndrome.

■    The outcome of  compartment syndrome depends on location and time to intervention.

■    Six hours of ischemia is currently the accepted upper limit of  viability.  Rorabeck  and  Macnab  reported almost  complete recovery of the limb function if fasciotomies are performed within 6 hours of the onset of symptoms.21

■    Muscle  undergoes irreversible change  after  8  hours  of ischemia, whereas nerves can have irreversible damage after as short as 6 hours.10

■    Compartment syndrome may have broad effects on multiple systems.

■    As  muscle necrosis occurs,  myoglobin,  potassium,  and other metabolites are released into circulation.

■    As a result, several metabolic conditions can arise, including myoglobinuria, hypothermia, metabolic acidosis, and hyperkalemia. In turn, these biochemical phenomena can cause renal failure, cardiac arrhythmias, and potentially death.

■    The use of physical examination findings to diagnose compartment syndrome has not been well validated.26  However, physical examination findings are widely used in clinical practice.

■    The key to successful handling of compartment syndrome is early diagnosis and  treatment. Therefore, the orthopedic surgeon must be familiar with the signs and symptoms of the diagnosis  and  perform  a  detailed documented history  and physical.

■    The  patient’s history is critical.  Certain  aspects of  the patient’s history may make the syndrome more likely.

■    The  existence  of  any  of  the  following   characteristics should heighten the surgeon’s suspicion: high-energy mechanism, a patient on anticoagulation, or a patient with a tight circumferential dressing.

■    A patient will often not demonstrate all of the classic “six Ps”:

pain, paresthesias, pulselessness, pallor, paralysis, and pressure.

■   Pulselessness  has recently been regarded as less of an indicator; patients can suffer extensive compartment syndrome with normal pulses.

■    Likewise, pallor reflects loss of arterial flow and is rarely present on physical examination.

■    Perhaps the most sensitive and earliest sign of compartment syndrome is pain  with  passive stretch of  the muscles of  the compartment.4

■    Pain out of proportion to the injury is also an early symptom of the diagnosis.

■    Pain may be absent if compartment syndrome is already established and nerve injury has occurred.

■    Since small fiber nerves are affected first, light touch will be affected before pressure and proprioception.

■    The ability to use pain as an indicator may be diminished in patients unable to sense pain or communicate with the caregivers; in this situation the surgeon must use other means to make the diagnosis.

■    Patients in whom pain may be difficult to ascertain include those with head injuries, those using ethanol or drugs, those who are intubated or sedated, those who have major distracting injuries such as a long bone fracture, those receiving large amounts of pain medicine, or any other factor that might alter the patient’s ability to accurately sense and communicate pain levels.

■    Pain perception may also be altered due to anesthesia, and some reports suggest that patients receiving epidural anesthesia are four  times more likely to  develop compartment syndrome than those receiving other forms of pain control.19

■    This  type  of  anesthesia results in  a  sympathetic nerve blockade,  thereby increasing the blood flow,  compounding the local tissue pressures and extremity swelling.

■    Similarly, local anesthesia combined with narcotics has been shown to increase the risk of compartment syndrome.6,19,20

■   Paresthesia  can be a useful, but confusing, symptom of compartment syndrome.

■    It has been shown, however, that nerve function is altered after only 2 hours of ischemia; therefore, it represents a potentially early symptom.8

■    With  increased pressure in  a  compartment,  the sensory nerves will be affected first, followed by the motor nerves (eg, in the anterior compartment, the deep peroneal nerve is affected quickly,  and patients will report loss of  sensation between the first two toes).

■    Paralysis is often less useful since it may be caused by ischemia, guarding, pain, or a combination of these factors, particularly in patients with a distracting extremity injury such as a tibial shaft fracture.

■    Serial examinations are critical. All complaints should be investigated thoroughly,  and  all  findings  should  be  carefully documented in the chart such that subsequent examiners can refer to the record as a tool for diagnosis (see Exam Table for Pelvis and Lower Extremity Trauma,  page 1).

■    Measurement of the compartment pressure

■    Stryker pressure monitor is most common (FIG  2).

■    Arterial line (16to 18-gauge needle) is easy to do in the operating room,  but the pressure measured with a simple needle is thought to be 5 to 19 mm Hg higher than the pressure measured with a side port or wick catheter.16

■    Pressure values should be recorded for all four compartments. Typically each compartment is checked twice. If there

FIG 2 • Stryker intracompartmental pressure monitor. A.  Quick pressure monitoring kit containing the intracompartmental pressure monitor, a prefilled saline syringe, a diaphragm chamber (transducer), and a needle. B. The assembled pressure monitor. To assemble the monitor kit, the needle is attached to the tapered end of the tapered chamber stem (transducer). The blue cap from the prefilled syringe is removed and the syringe is screwed into the remaining end of the transducer, which is a Luer-lock connection. The cover  of the monitor is opened. The transducer is placed inside the well (black  surface down). The snap cover  is closed. Next,  the clear  end cap is pulled off the syringe end, and the monitor is ready to use.  To prime the monitor, the needle is held at 45 degrees up from the horizontal and the syringe plunger is pushed slowly to purge air from the syringe. The monitor is then turned on.  The assembled monitor is tilted at the approximate intended angle of insertion of the needle into the skin. The zero button is pressed to zero the display. The needle is then inserted into the appropriate location in the compartment. C. The intracompartmental pressure monitor needle has side ports to prevent soft  tissue from collapsing around the needle opening.  This is different from a regular needle that has only one opening at the end.

is a fracture, the value is checked near and far from the fracture. The contralateral limb can be checked as a control.

■    Delta P (diastolic blood pressure minus intracompartmental pressure) is measured.

■    A delta P less than 30 mm Hg  is generally accepted as an indication for fasciotomy.  Compartment  syndrome is typically a clinical diagnosis and does not need measurement of the pressure before performance of fasciotomy.

■    Compartment  pressure checks should be reserved for patients who are difficult to examine, such as sedated patients or those with equivocal examination findings.

■    Tight compartments are an important indicator of compartment syndrome. The  deep posterior compartment cannot  be palpated directly because of its location deep to the superficial posterior compartment.

■    Pain with passive range of motion is one of the earliest and most important signs of compartment syndrome.

■    Decreased light touch is reported to be one of the first indicators of compartment syndrome. Light touch is a better indicator since it indicates change in the ability of the nerves to detect a threshold force, as opposed to two-point discrimination, which is a test of nerve density and may not change until later in the process.

■    Muscle  force  should  be documented in  all  compartments when ruling out  compartment syndrome. Documenting  that patient “wiggles  toes”  is not adequate as this indicates only

that  either the  flexor  or  extensor  hallucis  longus  is  firing. “NVI” is also not useful as it does not state the exact muscle groups that were tested.

■    The diagnosis of compartment syndrome is typically made clinically. There are, however, adjunct investigations that can be used to confirm or rule out the diagnosis.

■    Once  a patient is diagnosed with compartment syndrome, fasciotomies should  be  performed emergently. Any  workup that could delay this process should be undertaken with great caution.

■    If the patient cannot provide clinical clues because he or she is sedated or for other reasons, or if the diagnosis is in question, compartment pressures can be measured.

■    Several techniques to measure compartment pressures have been described, including the Whiteside infusion technique, the Stic technique, the Wick  catheter technique, and the slit catheter technique. The two most commonly used techniques are the Whiteside side port needle and the slit catheter device.

■    There are numerous commercially available digital pressure monitors that are frequently used as well.

■    The  exact  pressure that defines compartment syndrome is still debatable, although a measured pressure should be taken with reference to the diastolic blood pressure.13

■    McQueen et al did a prospective study on 116 tibial shaft fractures that  were monitored continuously  for  24  hours. They set the criterion for compartment release at a difference between diastolic  and  compartment pressures of  less than 30 mm Hg.  Following  this criterion, a total of  three had fasciotomies and none of the sample had late sequelae of compartment syndrome 9 months later.

■    The indications to measure compartment pressures include the following: one or more signs or symptoms of compartment syndrome and a confounding factor (eg, local anesthesia), unreliable examination  with  firmness in  an  injured extremity, prolonged hypotension and a swollen extremity with firmness, and spontaneous increase in pain after having received adequate analgesia.

■    The technique of measuring compartment pressures must be mastered by the surgeon.

■    Inexperience with the technique may lead to  inaccurate data and potentially missed compartment syndrome.

■    When measuring the pressure, the surgeon must be familiar with the local anatomy and able to accurately measure all of the compartments.

■    Location of the measurement is important.

■    Heckman et al reported the highest pressures were within

5 cm of the fracture site; pressures decreased as the measurements were taken distally and proximally to the fracture.27

They recommended that pressures be measured close to and both  distal  and  proximal  to  the  fracture in  all  compartments. The  highest measurement is compared to the diastolic blood pressure and interpreted accordingly.

■    Lab  studies should include a complete metabolic profile, a complete blood  count  with  differential,  creatine phosphokinase,  urine myoglobin,  serum myoglobin,  urinalysis (which may be positive for blood but negative for red blood cells, indicating myoglobin in the urine due to rhabdomyolysis), and a coagulation profile (prothrombin time, partial thromboplastin time, INR).

■    Obtaining  a complete laboratory panel should not delay operative treatment in  a  diagnosed  case of  compartment syndrome.

■    Compartment syndrome is diagnosed in a patient with either:

■    Suspicious clinical findings as discussed above, or

■   Pressure  in a compartment within 30 mm Hg  of the diastolic blood pressure

■    Other diagnoses to consider:

■    Normal   pain  response secondary  to  fracture  or  other trauma

■    Low  pain tolerance secondary to preoperative substance abuse

■    Muscle rupture

■    Deep venous thrombosis and thrombophlebitis

■    Cellulitis

■    Coelenterate and jellyfish envenomations

■    Necrotizing fasciitis

■    Peripheral vascular injury

■    Peripheral nerve injury

■    Rhabdomyolysis

■    Of  special note, in the case of envenomations, recent studies have shown that compartment syndrome is multifactorial and that fasciotomy may not prevent myonecrosis, which may be

due to the direct toxic effect of the venom and the inflammatory response.

■    In these cases, antivenom should be administered; this has been shown to decrease limb hypoperfusion.

■    All  patients suspected of  having  acute  compartment syndrome should  have emergent fasciotomies performed in  the operating room or at the bedside.

■    “Nonoperative” treatment of acute compartment syndrome is never appropriate, as this is a lifeand limb-threatening injury whose successful treatment is based on limiting the time until fasciotomy is performed.

■    Nonoperative  treatment of  compartment syndrome is reserved for patients presenting very late after a missed compartment  syndrome  who  already  have  irreversible muscle necrosis.

■    One school of thought is that these patients should not be débrided, as it will only increase the chance of infection.

■    This is controversial and applies only to chronic, missed compartment syndrome.

■    There is consensus that all acute compartment syndromes should be treated operatively with fasciotomies.

■    Since ischemic injury is the basis for compartment syndrome, additional oxygen should be administered to the patient diagnosed with  compartment  syndrome because it  will  increase slightly the blood partial pressure of oxygen (PO2).

■    The surgeon must ensure that the patient is normotensive,

as hypotension reduces perfusion pressure and leads to further tissue injury.

■    Any circumferential bandages or casts should be removed in patients at risk for development of compartment syndrome.

■    Compartment  pressure falls by 30%  when a cast is split on one side and by 65% when a cast is spread after splitting; splitting the padding reduces the pressure by an additional

10%,  complete removal of the cast by another 15%.  There could be a total of  85%  to 90%  reduction in pressure by just taking off the cast.28

■    Elevating the limb level above the heart decreases limb mean arterial  pressure without  changing  the  intracompartmental pressure. The affected extremity should not be elevated.

■    As shown by Styf and Wiger, after an elevation of 35 cm, the mean perfusion pressure decreased by 23 mm Hg but the intracompartmental pressure stayed the same.28

■    Intravenous fluids should be given to decrease the chance of kidney damage from myoglobin.

■    The “crush syndrome” is a sequela of muscle necrosis (ie, high  creatine phosphokinase  level,  above  20,000  IU)  and manifests as nonoliguric  renal failure,  myoglobinuria,  oliguria, shock, acidosis, hyperkalemia, and cardiac arrhythmias.

■    Treatment is supportive, with ventilatory support, hydration, correction of acidosis, and dialysis.

■    It is important in this situation to decrease the metabolic load by preventing ongoing tissue necrosis and débriding all dead tissue.

■    The use of narcotics should be closely recorded and monitored in any patient suspected of having compartment syndrome.

■    The use of local, spinal, or epidural anesthesia for postoperative pain control is generally discouraged in patients at high risk for compartment syndrome as it limits the ability of the clinician to do serial examinations.

■    All  patients with  acute compartment syndrome should be treated with emergent fasciotomies of  the affected compartments, as compartment syndrome is limb-threatening as well as potentially life-threatening if  allowed  to  progress to  myonecrosis and renal failure.

■    Time  to  diagnosis and surgical treatment of  compartment syndrome is critical, as nerve damage after 6 hours of ischemia may be irreversible.

■    Patients with compartment syndrome should be given the highest priority and treated as an operative emergency.

■    Fasciotomy of the involved compartment is the standard of care for compartment syndrome.

■    In a trauma setting, typically all four compartments of the leg are released, regardless of evidence of involvement of the other compartments.

■    Fasciotomies should ideally be performed in the operating room.

■    If the patient is too ill to be transported to the operating room or there is no operating room available, fasciotomies can be performed at the bedside in as sterile an environment as possible.

■    The  only  contraindication  to  fasciotomy  in  the face  of  a compartment syndrome is delayed presentation, in which a patient with missed compartment syndrome presents more than

24 to 48 hours after irreversible injury has set in.

■    Operative treatment is hypothesized to increase infection.

■    It is often difficult to know when a compartment syndrome occurred, however, so in situations in which it is unclear, it is probably wise to release the compartments.

■    One school of thought is that if the compartment syndrome has run its course, fasciotomies should not be performed unless the pressure in the compartment is within 30 mm Hg  of diastolic pressure.

■  Fasciotomies are also often performed in a prophylactic manner for any patient with an ischemic limb for more than 6 hours to prevent reperfusion injury.

■  Once  compartment syndrome is diagnosed, every effort should be directed at getting the patient to the operating room as quickly as possible for fasciotomies.

■    All  further workup should be deferred until fasciotomies are complete, except workup that is needed for a potential life-threatening injury.

■    There is little preoperative planning required for this component of the patient’s treatment.

■    Radiographs should be reviewed to rule out fractures or dislocations; however, additional radiographs can be taken in the operating room after fasciotomies have been completed.

■    Only  essential preoperative workup should be done before the patient is taken to the operating room, and the case should certainly  not  be  delayed  for  additional,  nonessential radiographic workup.

Positioning

■    The  patient is usually positioned supine on  the operating room  table to  facilitate fasciotomies. A  small bump may be placed under the affected hip.

■    The leg is prepared in a sterile fashion and a thigh tourniquet is applied but not inflated.

Approach

■    Two separate techniques have been used for decompression of the lower leg compartments.

■    The  two-incision  technique is the most commonly  used method, but a one-incision technique involving a lateral (perifibular) approach also exists.

■    The two-incision technique is more straightforward and requires less experience to ensure a complete compartment release and therefore is typically advocated.

■    Some have argued that the one-incision technique may be useful in defined anterior tibial artery injuries to help prevent loss of anterior skin.

Anterolateral Incision

■            The anterolateral incision decompresses the anterior and lateral compartments.

■       The  anterolateral  incision is made halfway between

the fibula and the crest   of  the tibia and lies  just above the intermuscular septum dividing the anterior and lateral compartments (TECH FIG 1A).

■            Fasciotomies have also been accomplished through small

incisions. However, we prefer using generous incisions to allow for  full decompression of the compartments.

■       We  recommend incisions that  are   typically at least

15 to 20 cm both medially and laterally.

■            A  small   transverse  incision  is  performed to  identify the  intermuscular septum,  after  which scissors   are used to  split   the  fascia   of   the  anterior and  lateral compartments.

■       Care  must be  taken to avoid injuring the superficial

peroneal nerve by making separate  incisions in each compartment and not cutting the intermuscular septum (TECH FIG 1B–F).

Posteromedial Incision

■            The  posteromedial approach decompresses the superficial and deep posterior compartments.

■       The incision lies about 2 cm posterior to the posterior

tibial margin (TECH FIG 2A).

■       Care  is taken to avoid injury  to the saphenous vein and nerve, which are  retracted anteriorly.

■            A small  transverse incision is made to allow visualization

of  the intermuscular septum between the deep and superficial posterior compartments, after which the fascia of  each is incised longitudinally in line  with the incision (TECH FIG 2B–E).

■            The  deep posterior compartment is initially released dis-

tally,   and  then  the  scissors   are   oriented  proximally through and under the soleus bridge.

■            It is crucial  to release the soleus attachment to the tibia

more than halfway. Also,  the fascia  over  the posterior tibial muscle should be  released.

■            One  useful tip  is to keep the tips  of  the scissors  away

from major neurovascular structures.

TECH FIG 1 • Lateral incision of the two-incision technique. A.  The anterolateral incision is made halfway between the fibula and the tibial crest  overlying the intermuscular septum dividing the anterior and lateral compartments. B. Close-up picture of the fasciotomy site  after skin incision before fascia  is open, showing the intermuscular septum between the lateral and anterior  compartments as well  as the course of the superficial peroneal nerve. C.  With  a knife, a small  transverse incision is made over  the intermuscular septum. Care  is taken to avoid injury  to the superficial peroneal nerve. D.  The surgeon inserts the tips of the scissors into the small  rent in the fascia, and keeping the tips  of the scissors up  and away from the superficial peroneal nerve, the surgeon incises the fascia  over  the anterior compartment distally. E. The scissors are  turned with the tips proximally, and the fascia  of the anterior compartment is released proximally. F. The tips of the scissors are  then inserted into the rent created in the fascia  of the lateral compartment. Keeping the tips of the scissors up and away from the superficial peroneal nerve, the surgeon releases the fascia  over  the lateral compartment proximal and distal.

                                                                                                    TECH FIG 2 • Medial incision of the two-incision technique.

A.  The medial incision lies about 2 cm posterior to the posterior  tibial margin. B.  Care  is taken to avoid injury  to the saphenous vein.  The  picture shows the posterior border of the tibia exposed along with the deep and superficial posterior  compartments. The  tips  of  the dissecting scissors  lie on the deep posterior compartment. C.  A small  transverse incision  is made to identify the intermuscular septum between the deep and superficial posterior compartments. Dissecting scissors are  used to release the fascia  over  the deep posterior compartment proximally and distally. Proximally the fascia  is released under the soleus bridge. Scissors are  shown under the fascia  of  the superficial posterior compartment. D.  The deep and superficial compartments are  released. The superficial   posterior compartment  looks   healthy,  whereas  the deep posterior compartment is dusky.  The tips  of the clamp lie under the soleus bridge, which also  needs to be  released from its  origin on  the tibia. E.  The  surgeon releases the soleus bridge using electrocautery, taking care  to protect theىdeep structures

                  

■            The  one-incision technique often requires more careful dissection around major neurovascular structures and can prove to be more challenging. For this reason it is less often used.

■            A straight lateral incision is created that originates just

posterior and parallel to the fibula at the level  of  the fibular head (protecting the peroneal nerve) to a point above the tip  of the lateral malleolus (TECH FIG 3A).

■            Posterior to the fibula, access  is gained to the deep and superficial posterior compartments (TECH FIG 3B).

■       The  fascia   between  the  soleus and  flexor hallucis

longus is identified distally and released proximally to the level  of the soleus origin (TECH FIG 3C).12

■            Anterior to the fibula, the anterior and lateral compart-

ments are  decompressed, taking care  to avoid injury  to the superficial peroneal nerve.

TECH FIG 3 • One-incision technique. A.  Schematic showing

the incision laterally just  posterior and parallel to the fibula. Again, care  is taken to avoid injury  to the superficial peroneal nerve. B.  Cross-section of  the mid-tibia showing dissection posterior to the fibula, allowing access  to the deep and superficial posterior compartments. Here  the fascia  between the soleus and flexor hallucis longus is identified distally and released proximally to the level of the soleus origin. C.  Schematic showing access  to the posterior tibia and thus release of the deep posterior compartment. Dissection anterior  to the fibula will allow identification of the intermuscular septum between the lateral and anterior compartments. The  fascia   overlying these  two  compartments is  released proximally and distally with the tips  of  dissecting scissors,

B   Gastrocnemius m.

taking care  to avoid injury  to the superficial peroneal nerve.

■            Regardless of  the choice of  fasciotomy performed, devitalized muscle is débrided as necessary.

■       Muscle   viability  is  ascertained  by  the  presence of

healthy color  and the ability to contract when pinched gently or touched with the electrocautery.

■       Necrotic muscle serves  no  function and must be  re-

moved eventually, as  it  will  form a  culture medium for  infection after fasciotomy.

■            Extensive débridement  is not typically undertaken until

the second look  at 36 to 72 hours, when muscle viability is more readily determined.

■            When fasciotomies are  performed in the setting of fractures, the fractures are  stabilized with either internal or external fixation, which eliminates the need for  constrictive  casts  and allows access  for  clinical  examination, repeat pressure measurements, and wound care.

■       Fixation of  fractures may  trigger  compartment  syn-

dromes through traction and reaming.

CLOSURE OF  FASCIOTOMIES

■            Fasciotomies are  typically not closed acutely because the skin itself  can  constrict muscle.

■            Most  often fasciotomy wounds are  either packed with

moist dressings (TECH FIG 4A)  or  covered with a sterile vacuum sponge and kept under suction until the next débridement (TECH FIG 4B).

■            Following a lower leg fasciotomy, a useful technique has

been the shoelace closure, which involves using a vessel loop and skin  staples to gradually close  large areas of gaping skin.

■       This allows gradual approximation of  the skin  edges

over  the course of several days,  thus potentially obviating the need for  a skin graft (TECH FIG 4C).

■            If two surgical wounds are  present, the surgeon should attempt to close  the medial wound secondarily before the lateral.

■       The lateral side of the leg has better soft  tissue cover-

age and consequently is easier to skin  graft over  if one of the wounds cannot be  closed.

■            Sometimes  small   relaxing  incisions around  the  fas-

ciotomy wound can  decrease the tension, enhancing the chance of healing (TECH FIG 4D).

TECH FIG 4  • Closure of  fasciotomies. A.  Moist  dressings covering the fasciotomy wound. B.  Sterile vacuum system applied to the fasciotomy site,  with vacuum suction set  between 100 and 125 mm  Hg. C. Small relaxing incisions made around the fasciotomy site to release tension and allow an easier closure. D.  Bootlace technique for  approximating the edges of a fasciotomy wound.

PEARLS AND PITFALLS

■  Medicolegal pitfalls: When in doubt, the surgeon should                 ■  In 1993  the average litigation award was  $280,000 for  eight measure and document pressure in all compartments of the               cases  of missed compartment syndrome (in all eight no involved extremity. The surgeon should clearly  document in                   compartment pressures were ever  measured).24

the patient’s chart that the patient does not have compartment syndrome at this  time if the clinical  examination findings and pressures are  negative.

■  The surgeon should consider the possibility of equipment                 ■  Needles can  be  misplaced in tendons, fascia, or wrong error.                                                                                                     compartment. All pressure readings must be  interpreted

within the context of the clinical  presentation.

■  The surgeon should fully release all four compartments along with the soleal leash and posterior tibial fascia.

■  No tight postoperative dressings should be  used.

■  Skin can  cause increased pressure, so the surgeon should not close  acutely.

■    Once  decompressed, the extremity should be covered in a bulky dressing, splinted with the foot in neutral, and elevated above the level of the heart to promote venous drainage and reduce interstitial fluid.

■    The foot should be splinted in neutral to prevent equinus contracture.

■    The patient must be closely monitored for the systemic effects of compartment syndrome. See the discussion in the nonopera-

tive section regarding administration of supplemental oxygen, intravenous hydration, mannitol, and hyperbaric oxygen.

■    Intravenous hydration is important to help prevent rhabdomyolysis,  as  discussed in  the  nonoperative  treatment section.

■    The  timing of  skin closure varies depending on  the cause and severity of compartment syndrome.

■    Most  fasciotomies can be closed in 5 to 7 days.

■    If   the  skin  is  not   easily  closed  secondarily,  a   splitthickness skin  graft  is  often  needed to  prevent excessive

granulation and to lessen exposure of muscle and tendon. A

flap may be needed if nerves, vessels, or bone is exposed.

■    If delayed primary closure is planned, small relaxing incision can be done.

■    Hyperbaric oxygen has been used because it reduces tissue edema through oxygen-induced vasoconstriction while maintaining and increasing oxygen perfusion.

■    However, its opponents argue that hyperbaric oxygen leads to reperfusion injury following compartment syndrome.

■    Other  agents that have been found to affect recovery from compartment syndrome include allopurinol  and  oxypurinol, superoxide dismutase, deferoxamine, and pentafraction of hydroxyethyl starch. These agents are antioxidants and scavenge for damaging free radicals.

OUTCOMES

■    Outcomes are generally poor if the compartment syndrome is diagnosed and treated in a delayed fashion. Results are better with earlier treatment.

■    In a study by Sheridan et al, 50%  of patients were decompressed within  12  hours and  50%  were decompressed after

12 hours.23   Sixty-eight percent of  the patients decompressed

within 12 hours had normal leg function, whereas only 8% of the delayed group had normal function.

■    If untreated, Volkmann ischemic contractures develop, leading to claw toes, weak dorsiflexors, sensory loss, chronic pain, and eventually amputation.

■    Most  patients (77%) complain of  altered sensation within the margins of the wound.13

■    Forty percent report dry, scaly skin, 33% pruritus, 30% discolored  skin,  25%  swollen  extremity,  26%  tethered scars,

13% recurrent ulcerations, 13% muscle herniation, 10% pain related to the wound, and 7% tethered tendons.

■   Severe  prolonged tissue ischemia resulting in necrosis of the muscles leads to fibrosis of the muscles and contracture that may continue over a period of several weeks.

■    This is known as Volkmann  ischemic contracture.

■    The late sequelae of compartment syndrome are weak dorsiflexors, claw toes, sensory loss, chronic pain, and eventually amputation.

■    Delayed fasciotomy after 12 hours has a reported infection rate of 46% and an amputation rate of 21%.23

■    The  complication  rate  for  delayed  fasciotomies  is  also much higher (54%) than that for early fasciotomies (4.5%). Therefore, the current recommendation is that if  the compartment syndrome has existed for more than 24 to 48 hours and the compartment pressures are not within 30 mm Hg of diastolic pressure, supportive treatment for acute renal failure should be considered, the skin is not violated, and plans should be made for a later reconstruction.

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